Macular Ganglion Cell -Inner Plexiform Layer Thickness Is Associated with Clinical Progression in Mild Cognitive Impairment and Alzheimers Disease.

Seong Hye Choi,Sang Jun Park,Na Rae Kim

doi:10.1371/journal.pone.0162202

Abstract

PurposeWe investigated the association of the macular ganglion cell-inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (RNFL) thicknesses with disease progression in mild cognitive impairment (MCI) and Alzheimer’s disease (AD).MethodsWe recruited 42 patients with AD, 26 with MCI, and 66 normal elderly controls. The thicknesses of the RNFL and GCIPL were measured via spectral-domain optic coherent tomography in all participants at baseline. The patients with MCI or AD underwent clinical and neuropsychological tests at baseline and once every year thereafter for 2 years.ResultsThe Clinical Dementia Rating scale-Sum of Boxes (CDR-SB) score exhibited significant negative relationships with the average GCIPL thickness (β = -0.15, p < 0.05) and the GCIPL thickness in the superotemporal, superonasal, and inferonasal sectors. The composite memory score exhibited significant positive associations with the average GCIPL thickness and the GCIPL thickness in the superotemporal, inferonasal, and inferotemporal sectors. The temporal RNFL thickness, the average and minimum GCIPL thicknesses, and the GCIPL thickness in the inferonasal, inferior, and inferotemporal sectors at baseline were significantly reduced in MCI patients who were converted to AD compared to stable MCI patients. The change of CDR-SB from baseline to 2 years exhibited significant negative associations with the average (β = -0.150, p = 0.006) and minimum GCIPL thicknesses as well as GCIPL thickness in the superotemporal, superior, superonasal, and inferonasal sectors at baseline.ConclusionsOur data suggest that macular GCIPL thickness represents a promising biomarker for monitoring the progression of MCI and AD.

Highlights

Alzheimer’s disease (AD) is the most common age-related dementia and is characterized by the accumulation of amyloid-β protein (Aβ) plaques as well as aggregates of hyperphosphorylated tau as neurofibrillary tangles in the brain.[1]
The temporal retinal nerve fiber layer (RNFL) thickness, the average and minimum ganglion cell-inner plexiform layer (GCIPL) thicknesses, and the GCIPL thickness in the inferonasal, inferior, and inferotemporal sectors at baseline were significantly reduced in mild cognitive impairment (MCI) patients who were converted to AD compared to stable MCI patients
Our data suggest that macular GCIPL thickness represents a promising biomarker for monitoring the progression of MCI and AD

Summary

Introduction

Alzheimer’s disease (AD) is the most common age-related dementia and is characterized by the accumulation of amyloid-β protein (Aβ) plaques as well as aggregates of hyperphosphorylated tau as neurofibrillary tangles in the brain.[1] The pathophysiological process of AD begins many years prior to detectable cognitive impairment.[2] The transitional phase is clinically recognized as preclinical AD and mild cognitive impairment (MCI).[2, 3] MCI has multiple etiologies and is categorized into amnestic and non-amnestic subtypes.[4] Amnestic MCI is considered a degenerative condition that may represent prodromal AD.[3] Recently, there has been a remarkable growth in AD biomarkers, including cerebrospinal fluid (CSF) measurement of a lower Aβ42 level, positron emission tomography (PET) amyloid imaging, and the assessment of medial temporal lobe atrophy via brain magnetic resonance imaging (MRI).[3, 5] researchers continue to search for new, less invasive and more cost-effective biological markers of AD.[6]

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